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  • 1
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    ATLASGAL - properties of compact H II regions and their natal clumps (2013)
    Oxford University Press
    Details
    Publication Date: 2013-09-17
    Description: We present a complete sample of molecular clumps containing compact and ultracompact H ii (UC H ii ) regions between  = 10° and 60° and | b | 〈 1°, identified by combining the APEX Telescope Large Area Survey of the Galaxy submm and CORNISH radio continuum surveys with visual examination of archival infrared data. Our sample is complete to optically thin, compact and UC H ii regions driven by a zero-age main-sequence star of spectral type B0 or earlier embedded within a 1000 M clump. In total we identify 213 compact and UC H ii regions, associated with 170 clumps. Unambiguous kinematic distances are derived for these clumps and used to estimate their masses and physical sizes, as well as the Lyman continuum fluxes and sizes of their embedded H ii regions. We find a clear lower envelope for the surface density of molecular clumps hosting massive star formation of 0.05 g cm –2 , which is consistent with a similar sample of clumps associated with 6.7 GHz masers. The mass of the most massive embedded stars is closely correlated with the mass of their natal clump. Young B stars appear to be significantly more luminous in the ultraviolet than predicted by current stellar atmosphere models. The properties of clumps associated with compact and UC H ii regions are very similar to those associated with 6.7 GHz methanol masers and we speculate that there is little evolution in the structure of the molecular clumps between these two phases. Finally, we identify a significant peak in the surface density of compact and UC H ii -regions associated with the W49A star-forming complex, noting that this complex is truly one of the most massive and intense regions of star formation in the Galaxy.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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  • 2
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    Development of a Continuous Flow System for the Oxidative Desulfurization of Refractory Organosulfur Compounds in Hydrotreated Diesel (2013)
    American Chemical Society (ACS)
    Details
    Publication Date: 2013-11-26
    Description: Energy & Fuels DOI: 10.1021/ef401708f
    Print ISSN: 0887-0624
    Electronic ISSN: 1520-5029
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Process Engineering, Biotechnology, Nutrition Technology
    Published by American Chemical Society (ACS)
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  • 3
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    Succinate is an inflammatory signal that induces IL-1beta through HIF-1alpha (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-29
    Description: Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis. Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1beta but not tumour-necrosis factor-alpha in mouse macrophages. A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and downregulation of mitochondrial genes, which correlates directly with the expression profiles of altered metabolites. Lipopolysaccharide strongly increases the levels of the tricarboxylic-acid cycle intermediate succinate. Glutamine-dependent anerplerosis is the principal source of succinate, although the 'GABA (gamma-aminobutyric acid) shunt' pathway also has a role. Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1alpha, an effect that is inhibited by 2-deoxyglucose, with interleukin-1beta as an important target. Lipopolysaccharide also increases succinylation of several proteins. We therefore identify succinate as a metabolite in innate immune signalling, which enhances interleukin-1beta production during inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031686/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031686/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tannahill, G M -- Curtis, A M -- Adamik, J -- Palsson-McDermott, E M -- McGettrick, A F -- Goel, G -- Frezza, C -- Bernard, N J -- Kelly, B -- Foley, N H -- Zheng, L -- Gardet, A -- Tong, Z -- Jany, S S -- Corr, S C -- Haneklaus, M -- Caffrey, B E -- Pierce, K -- Walmsley, S -- Beasley, F C -- Cummins, E -- Nizet, V -- Whyte, M -- Taylor, C T -- Lin, H -- Masters, S L -- Gottlieb, E -- Kelly, V P -- Clish, C -- Auron, P E -- Xavier, R J -- O'Neill, L A J -- 098516/Wellcome Trust/United Kingdom -- R01 AI093451/AI/NIAID NIH HHS/ -- R56 AI090863/AI/NIAID NIH HHS/ -- U54 AI057153/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- England -- Nature. 2013 Apr 11;496(7444):238-42. doi: 10.1038/nature11986. Epub 2013 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23535595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology ; Citric Acid Cycle/drug effects ; Deoxyglucose/pharmacology ; Down-Regulation/drug effects ; Genes, Mitochondrial/drug effects/genetics ; Glutamine/metabolism ; Glycolysis/drug effects/genetics ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism ; Immunity, Innate/drug effects ; Inflammation/metabolism ; Interleukin-1beta/*biosynthesis/genetics ; Lipopolysaccharides/pharmacology ; Macrophages/cytology/drug effects/metabolism ; Mice ; *Signal Transduction ; Succinic Acid/*metabolism ; Up-Regulation/drug effects ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    MET is required for the recruitment of anti-tumoural neutrophils (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-05-20
    Description: Mutations or amplification of the MET proto-oncogene are involved in the pathogenesis of several tumours, which rely on the constitutive engagement of this pathway for their growth and survival. However, MET is expressed not only by cancer cells but also by tumour-associated stromal cells, although its precise role in this compartment is not well characterized. Here we show that MET is required for neutrophil chemoattraction and cytotoxicity in response to its ligand hepatocyte growth factor (HGF). Met deletion in mouse neutrophils enhances tumour growth and metastasis. This phenotype correlates with reduced neutrophil infiltration to both the primary tumour and metastatic sites. Similarly, Met is necessary for neutrophil transudation during colitis, skin rash or peritonitis. Mechanistically, Met is induced by tumour-derived tumour necrosis factor (TNF)-alpha or other inflammatory stimuli in both mouse and human neutrophils. This induction is instrumental for neutrophil transmigration across an activated endothelium and for inducible nitric oxide synthase production upon HGF stimulation. Consequently, HGF/MET-dependent nitric oxide release by neutrophils promotes cancer cell killing, which abates tumour growth and metastasis. After systemic administration of a MET kinase inhibitor, we prove that the therapeutic benefit of MET targeting in cancer cells is partly countered by the pro-tumoural effect arising from MET blockade in neutrophils. Our work identifies an unprecedented role of MET in neutrophils, suggests a potential 'Achilles' heel' of MET-targeted therapies in cancer, and supports the rationale for evaluating anti-MET drugs in certain inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594765/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finisguerra, Veronica -- Di Conza, Giusy -- Di Matteo, Mario -- Serneels, Jens -- Costa, Sandra -- Thompson, A A Roger -- Wauters, Els -- Walmsley, Sarah -- Prenen, Hans -- Granot, Zvi -- Casazza, Andrea -- Mazzone, Massimiliano -- 098516/Wellcome Trust/United Kingdom -- 308459/European Research Council/International -- G0802255/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jun 18;522(7556):349-53. doi: 10.1038/nature14407. Epub 2015 May 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; 1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium [3] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal [4] ICVS/3B's - PT Government Associate Laboratory, 4710-057 Braga/Guimaraes, Portugal. ; Department of Infection and Immunity, University of Sheffield, Sheffield S10 2RX, UK. ; 1] Respiratory Division, University Hospital Gasthuisberg, Leuven B3000, Belgium [2] Laboratory of Translational Genetics, Vesalius Research Center, VIB, Leuven B3000, Belgium [3] Laboratory of Translational Genetics, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Digestive Oncology Unit, University Hospital Gasthuisberg, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University, Jerusalem 91120, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25985180" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Animals ; Antineoplastic Agents/*adverse effects/*pharmacology ; Disease Models, Animal ; Disease Progression ; Female ; Gene Deletion ; Hepatocyte Growth Factor ; Humans ; Inflammation/immunology/pathology ; Male ; Mice ; Middle Aged ; Neoplasm Metastasis ; Neoplasms/drug therapy/*immunology/*metabolism/pathology ; Neutrophils/drug effects/*immunology/secretion ; Nitric Oxide/secretion ; Proto-Oncogene Proteins c-met/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Solubility ; Transendothelial and Transepithelial Migration ; Tumor Necrosis Factor-alpha/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
    Electronic Resource
    Electronic Resource
    Soldier defense secretions of the south american termites Cortaritermes Silvestri, Nasutitermes SP N.D and Nasutitermes Kemneri
    Amsterdam : Elsevier
    Tetrahedron 38 (1982), S. 1899-1910 
    Details
    ISSN: 0040-4020
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0040-4020(82)80039-2
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Soldier defense secretions of the south american termites Cortaritermes Silvestri, Nasutitermes SP N.D and Nasutitermes Kemneri
    Amsterdam : Elsevier
    Tetrahedron 38 (1982), S. 1899-1910 
    Details
    ISSN: 0040-4020
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0040-4020(82)80039-2
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    In vitro susceptibility of“Campylobacter upsaliensis” to twenty-four antimicrobial agents (1990)
    Springer
    European journal of clinical microbiology & infectious diseases 9 (1990), S. 822-824 
    Details
    ISSN: 1435-4373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The in vitro susceptibility of 41 strains of“Campylobacter upsaliensis” to 24 antimicrobial agents was determined using a broth microdilution procedure. Most isolates were susceptible to the fluoroquinolones and β-lactam antibiotics tested, but all strains were resistant to trimethoprim (MBCs ≥ 128 µg/ml) and teicoplanin (MBCs ≥ 32 µg/ml). These agents may be useful in a selective isolation medium for“Campylobacter upsaliensis”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01967382
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  • 8
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    The Recombinant Hepatitis B Surface Antigen Vaccine in Persons With HIV: Is Seroconversion Sufficient for Long-term Protection? (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-25
    Description: A cohort of human immunodeficiency virus (HIV)–infected individuals with documented vaccine-induced hepatitis B surface antibody (HBsAb) seroconversion was evaluated retrospectively to determine factors associated with loss of protective levels of HBsAb. After a median follow-up of 43 months, 111 of the 152 participants (73%) maintained protective levels of HBsAb. HIV RNA suppression at vaccination was associated with persistence of protective levels of HBsAb (odds ratio, 3.83; P  〈 .01). Booster doses were provided for those with loss of protective antibody levels, and hepatitis B virus–specific immune memory, as evaluated with T-cell proliferation assays, was poor despite the observation that boosters successfully reinduced protective levels of HBsAb.
    Print ISSN: 0022-1899
    Electronic ISSN: 1537-6613
    Topics: Medicine
    Published by Oxford University Press on behalf of The Infectious Diseases Society of America (IDSA).
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  • 9
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    Cezanne Regulates Inflammatory Responses to Hypoxia in Endothelial Cells by Targeting TRAF6 for Deubiquitination [Integrative Physiology] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-06-07
    Description: Rationale: Hypoxia followed by reoxygenation promotes inflammation by activating nuclear factor B transcription factors in endothelial cells (ECs). This process involves modification of the signaling intermediary tumor necrosis factor receptor–associated factor 6 with polyubiquitin chains. Thus, cellular mechanisms that suppress tumor necrosis factor receptor–associated factor 6 ubiquitination are potential therapeutic targets to reduce inflammation in hypoxic tissues. Objective: In this study, we tested the hypothesis that endothelial activation in response to hypoxia-reoxygenation can be influenced by Cezanne, a deubiquitinating enzyme that cleaves ubiquitin from specific modified proteins. Methods and Results: Studies of cultured ECs demonstrated that hypoxia (1% oxygen) induced Cezanne via p38 mitogen–activated protein kinase–dependent transcriptional and post-transcriptional mechanisms. Hypoxia-reoxygenation had minimal effects on proinflammatory signaling in unmanipulated ECs but significantly enhanced Lys63 polyubiquitination of tumor necrosis factor receptor–associated factor 6, activation of nuclear factor B, and expression of inflammatory genes after silencing of Cezanne. Thus, although hypoxia primed cells for inflammatory activation, it simultaneously induced Cezanne, which impeded signaling to nuclear factor B by suppressing tumor necrosis factor receptor–associated factor 6 ubiquitination. Similarly, ischemia induced Cezanne in the murine kidney in vascular ECs, glomerular ECs, podocytes, and epithelial cells, and genetic deletion of Cezanne enhanced renal inflammation and injury in murine kidneys exposed to ischemia followed by reperfusion. Conclusions: We conclude that inflammatory responses to ischemia are controlled by a balance between ubiquitination and deubiquitination, and that Cezanne is a key regulator of this process. Our observations have important implications for therapeutic targeting of inflammation and injury during ischemia-reperfusion.
    Keywords: Cell signalling/signal transduction, Endothelium/vascular type/nitric oxide
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 10
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    Mutations in succinate dehydrogenase B (SDHB) enhance neutrophil survival independent of HIF-1{alpha} expression (2016)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2016-05-27
    Keywords: Phagocytes, Granulocytes, and Myelopoiesis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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